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TMAO? LMAO.

Move over saturated fat and cholesterol. There’s a new kid on the heart disease block: TMAO.

TMAO is not, as I first suspected, a new internet acronym that I was going to have to get my kids to decipher for me, while they snickered under their collective breaths. Rather, TMAO stands for Trimethylamine N-oxide, and it is set to become the reigning king of the “why meat is bad for you” argument. Former contenders, cholesterol and saturated fat, have apparently lost their mojo. After years of dominating the heart disease-diet debate, it turns out they were mere poseurs, only pretending to cause heart disease, the whole time distracting us from the true evils of TMAO.

The news is, the cholesterol and saturated fat in red meat can no longer be held responsible for clogging up your arteries. TMAO, which is produced by gut bacteria that digest the carnitine found in meat, is going to gum them up instead. This may be difficult to believe, especially in light of the fact that, while red meat intake has declined precipitously in the past 40 years, prevalence of heart disease has continued to climb. However, this is easily accounted for by the increase in consumption of Red Bull—which also contains carnitine—even though it is not, as some may suspect, made from real bulls (thank you, BW).

Here to explain once again why we should all be afraid of eating a food our ancestors ignorantly consumed in scandalous quantities (see what happened to them? they are mostly dead!) is the Medical Media Circus! Ringleader for today is the New York Times’ Gina Kolata, who never met a half-baked nutrition theory she didn’t like (apparently Gary Taubes’ theory regarding carbohydrates was not half-baked enough for her).

Step right up folks and meet TMAO, the star of “a surprising new explanation of why red meat may contribute to heart disease” (because, frankly, the old explanations aren’t looking too good these days).

We know that red meat maybe almost probably for sure contributes to heart disease, because that wild bunch at Harvard just keeps cranking out studies like this one, Eat Red Meat and You Will Die Soon.

This study and others just like it definitely prove that if you are a white, well-educated, middle/upper-middle class health professional born between 1920 and 1946 and you smoke and drink, but you don’t exercise, watch your weight, or take a multivitamin, then eating red meat will maybe almost probably for sure increase your risk of heart disease. With evidence like that, who needs evidence?

Flying like the Wallenda family in the face of decades of concrete and well-proven assumptions that the reason we should avoid red meat is because of its saturated fat and cholesterol content, the daring young scientists who discovered the relationship between TMAO and heart disease “suspected that saturated fat and cholesterol made only a minor contribution to the increased amount of heart disease seen in red-meat eaters” [meaning that is, the red-meat eaters that are white, well-educated, middle/upper-middle class health professionals, who smoke and drink and don’t exercise, watch their weight, or take a multivitamin; emphasis mine].

Perhaps their suspicions were alerted by studies such as this one, that found that, in randomized, controlled trials, with over 65 thousand participants, people who reduced or changed their dietary fat intake didn’t actually live any longer than the people who just kept eating and enjoying the same artery-clogging, saturated fat- and cholesterol-laden foods that they always had. (However, this research was able to determine that a steady diet of broiled chicken breasts does in fact make the years crawl by more slowly.)

Exactly how TMAO increases the risk of heart disease, nobody knows. But, good scientists that they are, the scientists have a theory. (Just to clarify, in some situations the word theory means: a coherent group of tested general propositions, commonly regarded as correct. This is not one of those situations.) The researcher’s think that TMAO enables cholesterol to “get into” artery walls and prevents the body from excreting “excess” cholesterol. At least that’s how it works in mice. Although mice don’t normally eat red meat, it should be noted that mice are exactly like people except they don’t have Twitter accounts. We know this because earlier mouse studies allowed scientists to prove beyond the shadow of a doubt that dietary cholesterol and saturated fat cause heart disease mice definitely do not have Twitter accounts.

Look, just because the scientists can’t explain how TMAO does all the bad stuff it does, doesn’t mean it’s not in there doing, you know, bad stuff. Remember, we are talking about molecules that are VERY VERY small and really small things can be hard to find–unless of course you are on a scientific fishing expedition.

What will happen to the American Heart Association’s seal of approval now that saturated fat and cholesterol are no longer to be feared?

Frankly, I’m relieved that we FINALLY know exactly what has been causing all this heart disease. Okay, so it’s not the saturated fat and cholesterol that we’ve been avoiding for 35 years. Heck, everybody makes mistakes. Even though Frank Sacks and Robert Eckel, two scientists from the American Heart Association, told us for decades that eating saturated fat and cholesterol was just greasing the rails on the fast track to death-by-clogged-arteries, they have no reason to doubt this new theory. And even though they apparently had no reason to doubt the now-doubtful old theory, at least not until just now—as a nation, we can rest assured that THIS time, they got it right.

Now that saturated fat and cholesterol are no longer Public Enemies Number One and Two, whole milk, cheese, eggs, and butter—which do not contain red meat—MUST BE OKAY! I guess there’s no more need for the AHA’s dietary limits on saturated fat, or for the USDA Guidelines restrictions on cholesterol intake, or for those new Front of Package labels identifying foods with too much saturated fat. Schools can start serving whole milk again, butter will once again be legal in California, and fat-free cheese can go back to being the substance that mouse pads are made out of. Halla-freaking- looyah! A new day has dawned.

But—amidst the rejoicing–don’t forget: Whether we blame saturated fat or cholesterol or TMAO, meat is exactly as bad for you now as it was 50 years ago.

The problem with the proliferation and debunking of these bad theories about food is the confusion they create out here in the hinterland. Health care professionals continue to spout the bad, old theories, along with all the new ones that come along.

Two weeks ago, I had one of those biometric health screenings offered through my workplace, because it gets me a discount on my health insurance. Since I had a slightly higher cholesterol than recommended (runs in my family), the nurse encouraged me to eat more beans in place of meat, since the one thing that’s been “proven” is that saturated fat causes heart disease. I argue that scientists don’t even really know what those readings mean, let alone show causation of heart disease.

At this point, I can ignore the results and walk away without a penalty. However, my workplace has been working for some years to give us a discount on our insurance based on the results of the tests, not just our willingness to take them. They are now offering points toward our discount if we meet with a health coach several times during the year. (During which they’ll keep spouting all the same bad advice I hear during the screenings, I’m sure.) It sure is frustrating to try to stay ahead of the BS.

My husband and I had one of those earlier this week. My numbers are all fine by mainstream standards so I didn’t get a lecture (which was good, bc after skipping breakfast to do fasting bloodwork, I was in NO mood). But the informational brochure was all conjecture and myth as usual. I took the time to fill out the customer service survey accordingly.

Hmmm. “Nutrition” huh? Wonder what you mean by that. The relationship between diet and chronic disease? Yeah, I would agree. It is absolutely far more complicated–or complex–than we are willing to admit. So complex, that–unless you are talking about deficiencies or toxicities–it is unlikely that we’ll be able to make any useful generalizations about it any time soon, if ever. On the other hand, if you are talking about nutrition as in “adequate” or “essential,” it’s really not all that complicated. Yes, genetic, environmental, and epigenetic differences will mean that there are differences in what will be adequate for any given individual, but right now, there is little controversy regarding what nutrients must be acquired from the diet in order to maintain health. In that regard, we can (and do) make sweeping generalizations about these essential (and non-essential) nutrients–then we turn right around and ignore them when it comes to making dietary recommendations.

Thanks for your humor. I have always believed that if butter was bad for us, it would taste bad! I mean, engineered food is engineered to taste good..but butter tastes so good …wait for it…because it does! I don’t eat meat because I don’t like to kill animals..and that little quirk does get in the way of eating them, LOL I do eat fish, however, because in my stunted mind I think they still have the chance to escape ( and please don’t disabuse me of that notion!) What I meant to say was this: eating what our ancestors ate can’t be BAD for us. Eating foods polluted with chemicals, heavy metals, meats/poultry/fish laced with antibiotics and hormones..these things can’t be GOOD for us. If folks want to eat red meat, they should do so with gusto, because our recent ancestors did so, and here we are:living longer and healthier than many thought possible. Our government should find better things to do with our money— no really!—think Michael Bloomberg..who’s idea of health promotion is to ban large soft drinks…but “please leave the Cheezits because I really like them.” Are you freakin’ kidding me? Yep, Adele, you’re a breath of fresh Southern air…

Thanks so much–y’know, Southerners have a remarkable ability to on the one hand, ignore every single shred of evidence of an elephant in a room including placing a doily on the dung heap and calling it an end table–yet, on the other hand, they sure can call a spade a freakin shovel (usually preceded by “bless his/her soul . . .) when it’s time.

A common expression, “Don’t quit your day job”, obviously does not logically apply in your case—I would pay good money to hear you present these sorts of painful, subversive ideas (as in: my sides are still aching from so much agreeable laughing) in stand-up formats. Too bad our current social realities cannot recognize the absurd rhetorical acrobatics of cultural gurus such as Gina Kolata.

On the other hand, I would love to read a critical analysis of Taubes’ explanation about “addiction” regarding carbohydrates. I’m convinced, based almost exclusively on personal experience, that adipose tissue (an endocrine producing organ) provides some compensatory mechanisms for those of us who “suffer from” or experience homeostatic imbalances in neurological (dopaminergic, specifically) neuro-endocrine dysregulations, aka illnesses primarily associated with dopamine-related brain function), which I believe are worsened by significant weight loss (adipose tissue depletion), and hence result in responses that resemble so-called “addictive” types of behaviors, as suggested by Taubes. Taubes and others would be far more helpful to those of us who struggle after significant adipose-tissue loss (aka weight loss) to more closely study the physiological (neuro-endocrine-metabolic) imbalances resulting from significant loss (shrinkage) of adipose tissue following low carbohydrate dieting.

For instance, I have had no problems with typical symptoms related to post weight loss via a low carbohydrate eating style, but my cognitive function still suffers as a result of (perhaps) insufficient Leptin (which, incidentally, assists with the brain’s optimal utilization of dopamine—especially for those of us whose brain functions are already compromised by inadequate dopamine function).

Clearly, these issues are far more complex than anything Kolata can include within her paradigm of nutritional infotainment. But some of us (more desperate—statistical outliers—are counting on researchers (Taubes?) to see beyond the rhetoric of “addiction” to the underlying neurological-endocrine imbalances created by adipose loss. Many of us face serious problems related to neuro-endocrine imbalances following the loss of adipose tissue. I hope (at least) some researchers are viewing these problematic results following so-called “weight loss” with the respect they (we) deserve.

Thanks for the kind words. According to my kids, I’m the funniest person I know.

Is the discussion on addiction you are referring to the one from GCBC?

You seem to know more about this than I do, but I think you may be onto something. In casual conversation with Rob Lustig about leptin a few years back, I asked him what he thought recovery time from carbohydrate-induced insulin/leptin dysregulation might be. We went back and forth about it a bit–the truth is that we don’t really know, but we were trying to make some educated guesses–and the time frame seemed to be around 7 years. Until then, it is very possible that many of the neurological issues related to leptin/insulin dysregulation (cravings, addictive behavior, depression, disordered eating) would remain. If BDNF, responsible for regulating neurogenesis, is part of this dysregulation–and there’s some indication that it would be–then cognitive repercussions might remain as well.

Now that I actually know more about insulin resistance at the blood-brain barrier and BDNF activity as it relates to CNS insulin levels, I think it is possible that, even on a low-carb diet, that BBB insulin resistance may remain. In a similar fashion, we had patients who, even on a low-carb diet, simply continued to pump out insulin in massive quantities. Needless to say, they didn’t lose weight. I think sometimes a metabolic cascade gets triggered and either becomes self-reinforcing or stuck in some other way & there’s no simple way to throw the switch back. But I hadn’t really thought about how that may be related to adipose tissue signalling.

I’m afraid it wouldn’t do much good for Taubes to study those things until somebody else studies them first. 🙂 I’m not sure we have enough science already in place for him to pick apart.

So, I’ve been working on balancing my hormones with supplements/diet for about 1 1/2 years now. That means I have about 5 1/2 years to go before I can consider my leptin in working order and MAYBE the fat will begin to naturally melt off? SIGH! I guess that’s better than nothing . . . a tiny pinhole of light at the end of the tunnel!

Well, I’m about to squelch it. Okay, not really, but if you haven’t had your insulin checked, I would strongly recommend finding a health professional that will help you figure out what is going on with that. You need that piece of information to make sense of everything else. Take your time & be picky about it. Metformin or octreotide may be in order to help the “reset.” In the meantime, think about the extent to which your weight and health goals are intertwined. For older adults, the things you have to do to lose weight may also comprise health. Just something to consider.

It sounds like you’re feeding yourself well, so maybe focus on some of the other facets of health, esp stress levels, for a change of pace 🙂

Already have a GREAT medical doc that has a degree in natural nutrition and treats as naturally as possible. Have had all the blood labs done 3 times so far. Insulin comes into normal range (both resistance and blood glucose) very easily when I stick to paleo. Grain raises everything to scary levels once more and very quickly, so I know I have to stay away from those. Once insulin is truly under control, to where I can eat a carby meal and not have everything blow up again, I think my leptin should begin functioning. I was just hoping all this would happen faster than 7 years.

But it is what it is. Maybe sooner, maybe later. Working on health first, weight loss second, but tracking both. Just NOT counting and stressing any longer. Trying to “just eat” the healthy things that make me feel and function better.

Please understand, without the Taubes’ concise explanations about the endocrinology of weight and weight loss, I would not have attempted the radical dietary changes (increased saturated fat, eliminated most grains, increased red meat, eggs, follow mildly ketogenic macro) that eventually lead to a loss of about 130 lbs. But those were not merely pounds of inert tissue. They were most pounds of ADIPOSE tissue, which is a primary endocrine organ responsible for producing and interacting with a host of hormones and neurotransmitters. Thus, the adipose tissue that shrank in mass so significantly during weight loss, no longer functions (does not meet my cognitive requirements) in a healthy, balanced way in terms of (in my case, neuro-endocrine function). Granted, a different weight-loss approach (a more *traditionally status quo*) would have left me ravenous and equally neurologically impaired, and I would have given up before losing even a modest (10%-15%), then regained it. So, I’m not blaming the KIND of weight-loss diet that MOST effectively produces statistically significant losses.

I’m suggesting that researchers and science writers (including Taubes, as far as I know) are focusing so intently on the EXTERNAL SUCCESSES RELATED TO LOSS OF WEIGHT and to the reduced rates of diabetes, for example, that they overlook the MAJOR KIND OF BODY WEIGHT TISSUE (adipose, aka vital endocrine tissue) that is “lost” (actually, the adipose cells shrink in mass though not in number.) Where is the research that compares adipose cell functioning before and after reduction in size?

Currently, I am attempting to refeed (umm, stuff) my *normal size* body with massive amounts of calories (lots of melted brie on ham, cans of macadamia nuts, butter, cream, etc) in an attempt to regain some of the weight (adipose tissue) I’ve lost. I’m hoping to increase adipose tissue mass whereby some of my previous cognitive function (executive function, specifically) may be restored through improved Leptin signalling between neurotransmitters (primarily dopamine). These (challenging) efforts to increase adipose mass are unrelated to appetite/hunger signalling—which most people seem to focus on as the critical role of endocrine-neuronal pathways involving adipose tissue.

I hypothesize here, and elsewhere, that one of the reasons SOME people are more prone to get fat in the first place relates to the compensatory cognitive benefits provided by increased adipose tissue and the corresponding increase (towards homeostasis) in endocrine functions as a means of providing neurological augmentation of key neurotransmitters in different parts of the brain. For me, as a life-long survivor of complex, chronic PTSD and ADHD (to borrow from inadequate psych terminology), I’ve found myself in a rather unique position to critically understand much of the the bullshit between our culture’s need to puritanically-blame-individuals-for-self-inflicted-immoral-behaviors and individual’s noble attempts to help themselves feel more *normal* and *well* and *functional* (as opposed to chronically sick and impaired) even though their actions (some would call *self medicating*) result in larger body sizes (with larger amounts of adipose tissue) which subject these people to painful bullying, discrimination and social stigma.

Many people don’t just regain their lost adipose mass because they give in to addictive-type, self-soothing, or emotional eating—they regain because they want to feel NORMAL, they want to think clearly again, they want to have more sense of energy and vitality and emotional stability…all those things that weight-loss propaganda is so good at promising and so inept at delivering in the long run.

I agree that a lot more needs to be done in the area of understanding what is happening throughout the body when weight is gained and lost. If the metabolic dysfunction precedes the accumulation of adipose, but then adipose adds its own metabolic “twist,” the metabolic states of pre-gain, gaining, weight stable (but with extra adipose), adipose-losing, and post-loss are likely to be very different from each other. It’s hard to explain why so little research has been done in this area, but I think the most straightforward reason is–you’re right–no one really cares that much about the endpoint you’re concerned with. The assumption is that when a person who is overweight/obese reduces their body weight, that outcome is universally and uniformly a positive one.

The reason you posit that some folks may accumulate adipose more easily than others is far too nuanced to serve the purposes of most of the scientists and the science writers, which is to tell a story that “solves” the obesity crisis–in 500 words or less if you are a writer, and “with additional research needed” of course, if you are a researcher.

Adele, this is a killer post – no pun intended! Yes, I have to agree: heaps and heaps of peer-reviewed scientific literature has proven–at least, thus far–that mice do not have Twitter accounts.

“Decades of concrete and well-proven assumptions” —-> What a great line! Yes, those pesky well-proven *assumptions.*

You are not only spot-on with pointing out that no one seems to have realized that sat fat & cholesterol are somewhat “exonerated” here, but you do it with pinpoint accurate intelligence and really fiery humor. This post is gold. Seriously, your writing is usually brilliant in its pointing out the stunningly obvious (at least, obvious to anyone with a whit of working knowledge of biochem & physiology), and the hypocrisy of our modern healthcare system, but this one takes the cake. There’s nothing like sarcasm and righteous (and funny) indignation from someone with the intellectual and academic moxie to back it up.

The carnitine thing especially cracks me up because I’m finally getting my obese, diabetic parents to see the light about low-carb, *real food* diets, and I just mailed them a bottle of L-carnitine supplements! I had to emphasize to them that I’m not kidding when I say they should do the *exact opposite* of what the six o’clock news, Dr. Oz, and Diabetes Forecast magazine say to do.

BawdyWench just introduced me to your blogs this morning. OH MY!!! What a laugh I’ve had 😀 I truly appreciated your comments on the “eating just food”, though. I am about 125# over what I want to weigh and have been doing paleo/primal for quite a long while. Just can’t seem to find the right combination. Have read and read and read, yet no one seems to have the golden ticket. I am old, I am tired, I HATE HATE HATE exercise, mostly because I feel near to death after doing it (and while doing it). The other day I just finally GAVE UP! I will continue taking my supplements and eating as paleo as I can because at least I can maintain and just feel better. Grain makes me gain.

So, from now on, I am eating “just food”. When I get hungry, I’ll eat enough to take away the hungries. I don’t care what the mice eat or what it does to/for them. I don’t care how quickly red meat kills me. I’ll still eat broccoli, though not 9 1/2 cups of it (the thought makes my jaws ache!). Just food, hopefully not junk food, not too much processed food. I am going to die one of these days anyway. With all the prospects the government is trying to enact, how long do I want to deal with it anyway???

Thanks for the HUGE laugh this morning and that bright light of common sense. I am sure that lengthened my life by at least a few days – LOL!!!!!

There ya go! That common sense I was talking about. Plenty of good, healthy saturated fat, good clean protein, veggies (non starchy of course, and mostly from my own garden), a few berries. No stressing over a minor carb-fest meal, just back to common sense once more. Life can be good 😀

Yeah, that would better. I struggle with the whole “protein foods” nomenclature. It sounds sorta dumb. Back in the old days, we could just say “meat, poultry, fish, milk, cheese, butter.” I really want to call that category “animal products and the fats they rode in on” but I do recognize the need to suggest vegetarian options for protein. When I use it as patient education, I say “animal products and the fats that naturally come with them, or some combinations of grains, dairy, nuts, and legumes.” So-I’m still playing with it.

Whether or not it is healthy, we do it all the time. Ask any woman who has had a yeast infection after a round of antibiotics.

I wonder how it got past peer review. Weren’t the reviewers concerned about the effect of this study on the Consistent Public Health Message? Or did they assume–correctly–that no one would actually focus on the exculpation of sat fat/cholesterol because everyone would be in a feeding frenzy about how red meat is even more scary than it was before.

When I first read about the antibiotic intervention in this study, it reinforced my general impression that cardiologists are not so very much concerned with people’s overall health. They seem to be very narrowly focused on their own specialty and treatment modalities, to the point that it doesn’t matter how debilitated, diabetic, depressed, impotent, or in pain you are as long as your calculated LDL is below 70. A cardiologist once said to my husband, recommending statin therapy, “What’s a little muscle pain compared to not dying of a heart attack?” As if it were that simple, or guaranteed.

“As if it were that simple, or guaranteed.” This lack of professional humility–which may be pronounced in cardiologist, but is endemic to the health professions–is certainly one of the things that needs to be addressed. We know so much less than we pretend to know.

I am with Dr Feinman in that I do see something to take seriously in this; the concept, originated or at least promoted by Elie Metchnikoff circa 1904, that “bad” bacteria produce life-shortening toxins while fermenting the foods we eat and we should try to optimize our population of “good” bacteria, is not inherently ridiculous, and is worth investigating in every way.
These days there is probably more interest in LPS and other immune-stimulating fractions of bacteria, but we needn’t overlook the old-fashioned reductionist approach of looking for chemical toxins. As long as the effect of LPS was properly controlled for in this study.
At first blush, it’s hard to understand what the problem is with TMAO. Fish seems to be the richest source but no-one blames fish for CVD. TMAO is an osmolyte (like betaine and taurine) and protects proteins from stress (it counters the effect of urea), which is why sea creatures produce it. Carnitine – and possibly TMAO as a result – is elevated in conditions (like cardiomyopathy) where mitochondrial function is impaired.

I notice that carnitine was only associated with CVD in the study after a “hypothesis-driven” relaxing of the criteria initially set for its measurement.

Homocysteine is also one of these reductionist single-chemical “causes” of CVD, and homocysteine levels are higher in vegans and vegetarians than in meat eaters.
I’m sorry, but it looks as if, no matter what we eat, we might all have to die in the end. I don’t like it any more than you do, but that seems to be the inescapable conclusion.
The best we can hope to do is to go out in the style we are accustomed to, like Kurt Wallenda.

I come from a long & proud line of sauerkraut-eaters; my dad makes barrels of the stuff. I think there is much of interest in the study & much to be ridiculed in the way the media presented as the latest installment of food-fear-of-the-month.

We can take the science seriously without taking any of the publicity around it seriously at all & in fact, as a nation, I think we need to learn to do that. Part of what drives the media frenzy is that, as Richard has pointed out many times, the public is terribly confused about what to eat. The source of this confusion is the establishment of a national classification of regular old foods into “good” and “bad” categories without the requisite science (if there will ever be such a thing) to back up such designations. There was a time when “junk food” was bad for you (and everybody knew what it was and nobody pretended it was anything but junk, although we sometimes ate it anyway, if we could scrape together enough change from collecting the deposits from bottles we found on the side of the road) and all other non-junk food was good for you. (Ice cream always occupied a demilitarized zone of being a junk food that was okay to eat, mostly I think because all the grown ups still thought of ice cream as fabulous evidence of the wonders of modern refrigeration systems.)

Now granola bars, which are officially categorized as a “dessert” by NHANES, have labels that proclaim how “healthy” they are: whole grain, low fat, no cholesterol, protein, calcium–you name it and they’ve put it (or taken it out of) a granola bar. Granola bars are sort of the canary in the nutrition coal-mine. You’ll know what food fad is about to swamp the market because it shows up first on a box of granola bars. Look for “carnitine-free” granola bars, coming soon to a grocery store near you.

I don’t think we should dismiss the whole thing out of hand. This has some serious aspects outside of the prejudices of the authors, taking as established something that is conjecture at best and the mindless rush to judgement of the media. And, as pointed out in the old ADA merger report, giving apoE knockout mice atherosclerosis is the behavioral equivalent of training a cat to go to sleep. The study may show something about the metabolism of carnitine and it may be related if not causal in CVD. Just because of the incredible crap that we usually get about how red meat will kill you, we might not want to dismiss everything in this. I will look further.

I’m not dismissing the concept that microflora are important aspects of the relationship between diet and disease. I am (I hope) dismissing the media circus that, as Mark Shields pointed out, fell all over themselves about this new & improved version of death-by-red-meat, but failed to suggest that they might have been telling the wrong story for the last 35 years–or even really acknowledging at all that if the TMAO thing is valid (and Frank Sacks has no reason to doubt that it is), then the sat fat/cholesterol thing isn’t.

No, Hazen didn’t go far enough. If you are on a fishing expedition with the assumption at the outset that you want to find something that proves that red meat is bad, that’s the sort of fishing hole you’re going to fish in. That seems a little fishy to me 🙂

The question that intrigues me is what is the difference between the folks with the high carnitine levels and the folks with the high carnitine levels and high TMAO levels?

I think the answer to your question is a difference in the gut bacteria.
Thanks for the laughter. When I read the article in the NY Times, my first thought was, “Here they go again.” Then, “Will they ever stop with the meat thing?” Then, I just wondered why meat producers weren’t funding more research.

“I just wondered why meat producers weren’t funding more research.” Good point. When I hear all that nonsense about the meat industry controlling the USDA and manipulating our dietary recommendations & the minds of the public, I always think, if this is what the “beef lobbyists” have managed to accomplish (recommendations that become more plant-based every 5 years), their clients needs to ask for their money back.

I think the answer may be gut bacteria too, but how/why are the gut bacteria different?

I really do get tired of these scientists always trying to find something to scare us with, my guess is they need these scares to drum up taxpayer/corp funding, who knows maybe it is the greenies of the world who fund these things to scare people from eating meat and animal products (and thus become dependant on plant based diets which are proving to not be as nutrtious as they used to be) to weaken us maybe? why else would they keep touting garbage like this or outlaw herbs and thearaputice doses of vita and minerals and such? surly not to keep us healthy but tomake us weak and sick. and dependant on drugs. creeps,

I remember a time–I’m old, but it really wasn’t all that long ago–when we all Just Ate Food. Sometimes it was “real” food, sometimes it was surreal food (remember Freakies breakfast cereal?)–but mostly it was Just Food. We didn’t think about it all that strenuously. I’m not sure we can put that genie back in the bottle, but maybe we should at least try.

I like the analogy of the nutrition world with the Flying Wallendas. Without overdoing it, I can’t help thinking of the patriarch, Kurt Wallenda walking on a high wire in a high wind between two buildings in Sao Paolo, Brazil (presumably the only place that would let him do it) and falling to his death. It was not a suicide but rather, in old age, he simply wanted to go out doing his thing. Would that the lipophobes had such strength of character.

Well, first gut-wiping antibiotics. Then anti-fungals to counteract the opportunistic yeast infection. Then antacids to deal with the indigestion from the antifungals. Then either a laxative or whatever the opposite of a laxative is for either the constipation or the diarrhea from the antacids–and so on. The plan is for everyone to get screwed up enough metabolically so that our kidneys will fail & we’ll all be on dialysis, because dialysis is the perfect intervention. Takes a lot of medical personnel, equipment, supplies, time, and you are completely dependent on it till death do you part. Right now, we’re only managing to move people closer to dialysis from the diabetes care standpoint, which has limited our markets somewhat. So, of course, heart disease care is the obvious next step.